We have reported that animals fed a diet containing cyclocreatin accumulate high concentrations of cyclocreatin-3-P (1-carboxymethyl-2-imino-3-phosphonoimidazolidine), a synthetic analogue of creatine-P, in heart, skeletal muscle, and brain. We have recently observed that ischemic heart and skeletal muscle of rats, mice, and chicks containing this novel reservoir of high-energy phosphate have a markedly delayed onset of rigor. This indicates that intracellular energy stores are better maintained during prolonged ischemia with this synthetic phosphagen than with the natural phosphagen alone. On the basis of these results we propose that heart preloaded with cyclocreatin might better withstand surgical procedures and ischemic or anoxic episodes. Similarly, severed digits and limbs might survive longer periods prior to surgical restoration, and nerve tissues might better survive ischemic episodes, when preloaded with this synthetic reservoir of high-energy phosphate. We propose to determine: (a) the optimal experimental systems and dietary regimen for demonstration of delayed rigor; (b) the biochemical basis for rigor delay; and (c) whether intracellular energy stores in cyclocreatin-fed animals are better maintained during ischemic episodes short of rigor development. We shall employ methods developed in this laboratory for loading of organs with cyclocreatin-3-P and for its assay, and use standard assay methods for intracellular ATP, creatine-P, glycogen, and glycolytic intermediates during various experimental perturbations.